: Nilotinib is a second-generation tyrosine kinase inhibitor (TKI) targeting BCR/ABL, which is used for the first-line treatment of newly diagnosed chronic myeloid leukemia (CML) patients and the second-line treatment of most CML patients who are resistant or intolerant to prior therapy that includes imatinib. In addition to common adverse reactions, long-term use of nilotinib shows some toxicities that are different from those of occurring during other BCR/ABL TKI treatments, such as cardiovascular toxicity. It is life-threatening, which would affect not only the choice of initial treatment of CML patients but also the safety of long-term medication.: Through searching literature and reports from PubMed and clinical trials, here we review a profile of the adverse effects induced by nilotinib. We also discuss the potential molecular toxicological mechanisms and clinical management, which may provide strategies to prevent or intervene the toxicity associated with nilotinib.: Severe adverse effects associated with nilotinib limit its long-term clinical application. However, the exact mechanisms underlying these toxicities remain unclear. Future research should focus on the developing strategies to reduce the toxicities of nilotinib as well as to avoid similar toxicity in the development of new drugs.
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http://dx.doi.org/10.1080/17512433.2021.1894129 | DOI Listing |
BMC Neurol
January 2025
Department of Neurosurgery, Gifu University Graduate School of Medicine, 1-1, Yanagido, Gifu, 501-1194, Japan.
Background: Tyrosine kinase inhibitors (TKIs) improve prognosis in chronic myeloid leukemia (CML). Nilotinib and ponatinib, second- and third-generation TKIs, respectively, have been reported to cause adverse vascular occlusive events such as myocardial infarction and peripheral arterial disease. However, little is known about the risk of cerebral infarction associated with severe cerebrovascular stenosis, which is a late complication of TKIs.
View Article and Find Full Text PDFJ Hematol Oncol
December 2024
Georgia Cancer Center, Augusta, GA, USA.
Background: Up to 65% of patients with chronic myeloid leukemia (CML) who are treated with imatinib do not achieve sustained deep molecular response, which is required to attempt treatment-free remission. Asciminib is the only approved BCR::ABL1 inhibitor that Specifically Targets the ABL Myristoyl Pocket. This unique mechanism of action allows asciminib to be combined with adenosine triphosphate-competitive tyrosine kinase inhibitors to prevent resistance and enhance efficacy.
View Article and Find Full Text PDFPLoS One
November 2024
Bioinformatics Laboratory, Department of Statistics, University of Rajshahi, Rajshahi, Bangladesh.
Breast cancer (BC) is yet a significant global health challenge across various populations including Ghana, though several studies on host-genome associated with BC have been investigated molecular mechanisms of BC development and progression, and candidate therapeutic agents. However, a little attention has been given on microbial genome in this regard, although alterations in microbiota and epigenetic modifications are recognized as substantial risk factors for BC. This study focused on identifying bacterial key genes (bKGs) associated with BC infections in the Ghanaian population and exploring potential drug molecules by targeting these bKGs through in silico analyses.
View Article and Find Full Text PDFGeorgian Med News
September 2024
3College of Medicine, University of Sulaimani, Kurdistan region, Iraq.
Comb Chem High Throughput Screen
November 2024
Department of Respiratory and Critical Care Medicine, Changhai Hospital, Shanghai, China.
Purpose: The purpose of this study is to investigate the underlying relationship of diagnosis and therapy between glutamine-fructose-6-phosphate transaminase 2 (GFPT2) and various cancers.
Methods: The Cancer Genome Atlas (TCGA) database was utilized to get gene expression RNAseq and clinical data for 33 tumors. The immunotherapeutic cohorts, including GSE35640, GSE78220, GSE67501, GSE181815, and IMvigor210, were derived from the Gene Expression Omnibus database (GEO) and a previously released article.
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